ライフサイエンスコーパス: hepatoma

1 oncolytic Ad safely and efficiently to treat hepatoma.

2 ch has high affinity and selectivity towards hepatoma.

3 miR-21 and TIAM1 expression in patients with hepatoma.

4 d, malignant hepatocellular carcinoma Morris hepatoma 7777 was systematically optimized to yield the

5 4 (TLR4), TLR2, and erythropoietin-producing hepatoma A2 (EphA2) expression was significantly higher

6 The erythropoietin-producing hepatoma A2 receptor (EphA2) is a tyrosine kinase overex

7 was also shown that sesamol has potent anti-hepatoma activity in a xenograft nude mice model.

8 PHY906 may potentiate the anti-hepatoma activity of Sorafenib by multiple mechanisms ta

9 Co-cultures of human hepatoma and hepatic stellate (HSCs) cells were exposed

10 d migration, we used primary hepatocytes and hepatoma and macrophage cell lines.

11 al RNA transfer mechanism by human and mouse hepatoma and nonhepatoma cells that replicate the negati

12 ally altered in cachectic muscles of Yoshida hepatoma-bearing rodents but not in those with diabetes,

13 ABP-PEG-HCBP1 delivered oAd efficiently into hepatoma cancer cells.

14 ressing ad, (Ad/GFP)-ABP-PEG-HCBP1, showed a hepatoma cancer specific uptake and transduction compare

15 icantly decreased Met and VEGF expression in hepatoma cancer, but not in non-hepatoma cancer.

16 xpression in hepatoma cancer, but not in non-hepatoma cancer.

17 tis C virus (HCV) clones propagated in human hepatoma cell cultures yield relatively low infectivity

18 hyroid hormone receptor (TRalpha1) regulates hepatoma cell growth and pathophysiology, but the underl

19 assay showed that pEpo-AFPL-Luc transfected hepatoma cell increased gene expression under hypoxic co

20 in primary rat hepatocytes (PRHs) and human hepatoma cell line (HepG2) were quantified by dichlorofl

21 We found that JB12 was required in human hepatoma cell line 7 (Huh-7) liver cancer cells to maint

22 Hepatoma cell line and immortalized human hepatocytes tr

23 ment of a polarizable, HBV-susceptible human hepatoma cell line and studies of primary hepatocytes fr

24 but also in several cell lines: e.g., in the hepatoma cell line BWTG3, as evidenced by impaired Dexam

25 on of CYP1A1 mRNA and EROD activity in human hepatoma cell line Hep3B.

26 iver mitochondria and in the cultured murine hepatoma cell line Hepa1c1c7.

27 Removing serum from the medium of the human hepatoma cell line HepG2 increased Rdh10 and Rdh16 (huma

28 In the human hepatoma cell line HepG2, retinoic acid, clofibric acid,

29 e to efficiently block HCV attachment to the hepatoma cell line Huh-7.5 as well as primary human hepa

30 ls comparable to the highly permissive human hepatoma cell line Huh-7.5.

31 sly shown that confluent growth of the human hepatoma cell line Huh7 substantially induces the CYP3A4

32 In the human hepatoma cell line Huh7, the coexpression of the coactiv

33 In this study, we differentiated the human hepatoma cell line Huh7.5 by supplementing tissue cultur

34 We confirmed these findings in the human hepatoma cell line Huh7.5.1.

35 Transfection of 20 such mutants in a human hepatoma cell line identified many with severe impairmen

36 Transient overexpression of IFNL4 in a hepatoma cell line induced STAT1 and STAT2 phosphorylati

37 onversely, expression of LSP1 in the JM2 rat hepatoma cell line led to decreased proliferation.

38 tissue, and knockout of the CIDEB gene in a hepatoma cell line results in multiple aspects of lipid

39 of-function screen using a poorly permissive hepatoma cell line to uncover host factors enhancing HBV

40 hondrial and cellular response to alcohol in hepatoma cell line VL-17A.

41 e of QSG-7701 (human hepatocyte) with HepG2 (hepatoma cell line) increases QSG-7701's proliferation,

42 d in VA-13 cells, an EtOH-metabolizing human hepatoma cell line, which displayed marked defects in bo

43 hput screening performed in the Hepa-1 mouse hepatoma cell line, which revealed that SIN3A is necessa

44 egrades clathrin heavy chain expression in a hepatoma cell line.

45 ly knock down LSP1 expression in the JM1 rat hepatoma cell line.

46 BV and HDV receptor activity in a permissive hepatoma cell line.

47 d the aminoglycosides G418 and gentamicin in hepatoma cell lines (HepG2, Hep3B and Hepa1-6) and in ex

48 Three hepatoma cell lines (HepG2, Hepa-1, and Huh-7) were trea

49 Cell viability of two human hepatoma cell lines (Huh7 and Hep-G2) was quantitatively

50 In rat hepatoma cell lines and mouse liver in vivo, LSP1 functi

51 We confirm MUC13 transcript increases in hepatoma cell lines and primary hepatocytes.

52 f SMAD6 blocked the binding and infection of hepatoma cell lines and primary human hepatocytes by HCV

53 In studies of hepatoma cell lines and primary human hepatocytes, we fo

54 expression of bile acid homeostasis genes in hepatoma cell lines and primary human hepatocytes.

55 FQ potently inhibited HCV infection of hepatoma cell lines by affecting an early step of the vi

56 8(+) T cells in primary human hepatocyte and hepatoma cell lines either infected with HBV or harborin

57 HEV genotype 3 p6 (Kernow C-1) and the human hepatoma cell lines HepG2 and HepG2/C3A with different m

58 The pEpo-AFPL-TK was transfected into hepatoma cell lines in the presence of ganciclovir (GCV)

59 iment, we found that GLO1 knockdown in human hepatoma cell lines increased levels of cellular cholest

60 Finally, depletion of iron in the medium of hepatoma cell lines incubated with the iron chelator des

61 Hepatoma cell lines JM1 and JM2 have decreased CD81 expr

62 ilencing or inhibition of endogenous TAK1 in hepatoma cell lines leads to an upregulation of HBV repl

63 ing, but also that sterol depletion of human hepatoma cell lines reduced HNRNPA1 mRNA levels, an effe

64 (HBV) receptor enabled researchers to create hepatoma cell lines susceptible to HBV infection.

65 , decreased SIRT6 expression was observed in hepatoma cell lines that are known to be apoptosis-insen

66 ver models of infection typically use either hepatoma cell lines that exhibit aberrant physiology or

67 ndent tetracycline-inducible systems in four hepatoma cell lines with different p53 mutational status

68 silencing of SLC13A5 expression in two human hepatoma cell lines, HepG2 and Huh7, profoundly suppress

69 In human hepatoma cell lines, SUGP1 knockdown stimulated 3-hydrox

70 In both human and murine hepatoma cell lines, treatment with chemicals that stabi

71 imary human hepatocytes, liver biopsies, and hepatoma cell lines.

72 ver following partial hepatectomy (PHx), and hepatoma cell lines.

73 lication of diverse HCV genotypes in several hepatoma cell lines.

74 the miR-200 family were conducted using the hepatoma cell lines.

75 ding and infection were tested in transduced hepatoma cell lines.

76 titis B surface antigen (HBsAg) particles of hepatoma cell lines.

77 Overexpression of miR-21 promoted hepatoma cell migration and invasion, similar to that ob

78 3) and subsequent TIAM1 suppression promotes hepatoma cell migration and invasion.

79 ted that miR-224 played an oncogenic role in hepatoma cell migration and tumor formation through sile

80 ng hepatic energy homeostasis to influencing hepatoma cell proliferation and suggest a potential role

81 with 2-DG produces synergistic inhibition on hepatoma cell proliferation by dual targeting of apoptos

82 (Thr567) antagonist, significantly decreased hepatoma cell proliferation.

83 ts were given intrahepatic injections of rat hepatoma cells (H4IIE); 24 tumor-bearing rats (mean tumo

84 bling isolates of all HCV genotypes in human hepatoma cells (HCVcc), production efficacy varies.

85 ls (capital A, Cyrillic549) as compared with hepatoma cells (Hep3b).

86 tents, and reactive oxygen species levels in hepatoma cells (Hepa1-6), a promising approach for targe

87 lycoprotein (P-gp) encoded by ABCB1 in human hepatoma cells (HepG2) without modifying the expression

88 To this end, we exposed human hepatoma cells (Huh7) to 0.5 muM (nontoxic concentration

89 Conditioned medium from HCV-infected hepatoma cells (Huh7.5 cells) or immortalized human hepa

90 Coculture of NK cells (NK3.3) with human hepatoma cells (Huh7.5) expressing HCV core or NS5A prot

91 atoma cells (JFH-1), and not with uninfected hepatoma cells (Huh7.5), induced IFN-alpha production.

92 icity of HCV-infected HLA-A2-positive Huh7.5 hepatoma cells (Huh7.5A2 cells) in activating HCV-specif

93 nant hepatitis type 1 (JFH-1) virus-infected hepatoma cells (JFH-1), and not with uninfected hepatoma

94 comprehensive peptidome from GPC3-expressing hepatoma cells after immune-affinity purification of hum

95 e effect of PD-L1 expression on HCV-infected hepatoma cells against HCV-specific CD8 T cells.

96 DCLK1 overexpression in hepatoma cells also increased phosphorylation of GSK-3be

97 interact transiently on membrane tubules in hepatoma cells and along LD-centric autophagic membranes

98 expressed these mutants in engineered murine hepatoma cells and although we observed increases in HCV

99 culture-derived HCV-producing Huh7.5-derived hepatoma cells and confirmed its depletion by immunoblot

100 SMAD (SMAD7) promote HCV infection in human hepatoma cells and hepatocytes.

101 ed completion of the HCV infectious cycle in hepatoma cells and HFLCs in a dose-dependent and time-de

102 n, entry, spread, production, and release in hepatoma cells and HFLCs.

103 search for FXR-interacting proteins in human hepatoma cells and identified AMPK as a coregulator of F

104 In human Hep3B hepatoma cells and in EPO-generating organs of hypoxic o

105 transporter mRNA levels were assessed in rat hepatoma cells and in mice by peptide injection or adeno

106 w that down-regulation of C/EBPbeta in mouse hepatoma cells and in mouse livers reduces C/EBPbeta-HDA

107 icient to cause hepcidin suppression in Huh7 hepatoma cells and in wild-type mice.

108 o increase entry of HCV pseudoparticles into hepatoma cells and inhibit signaling by interferon alpha

109 at Nox4 mediates LPS-TLR4 signaling in human hepatoma cells and murine hepatocytes and may contribute

110 F on HCV infection of and spread among Huh-7 hepatoma cells and primary HFLCs.

111 the proteasome inhibitor bortezomib (BZB) in hepatoma cells and primary human hepatocytes as well as

112 responses induced by these cytokines in Huh7 hepatoma cells and primary human hepatocytes.

113 H4IIE hepatoma cells and rat primary hepatocytes were incubate

114 LDL-DHA nanoparticle selectively kills hepatoma cells and reduces growth of orthotopic liver tu

115 cytotoxicity and potency toward Nrf2 in rat hepatoma cells and stably modifies specific cysteine res

116 Overexpression of KIF18B and CDCA3 in hepatoma cells and subsequent microarray analysis reveal

117 Nox4) in LPS-induced TLR4 responses in human hepatoma cells and wildtype and Nox4-deficient mice.

118 iosynthesis, as PGRMC1 depletion in cultured hepatoma cells and zebrafish blocked the ability of HISs

119 ed in subsequent biological studies on mouse hepatoma cells as it easily crosses the cell membrane an

120 aVpu virus release from BST-2-positive HepG2 hepatoma cells but not HeLa cells, whereas Vpu failed to

121 were determined in plasma phospholipids and hepatoma cells by gas chromatography.Cellulose did not a

122 l data show that recognition of HCV-infected hepatoma cells by pDCs involves CD81- and CD9-associated

123 nificant increasing of death rate in hypoxic hepatoma cells compared to controls.

124 t hairpin RNA-mediated attenuation of ISX in hepatoma cells decreased cell proliferation and malignan

125 ll-derived hepatocyte-like cells (HLCs), and hepatoma cells exhibit poor drug biotransformation capac

126 docytic cycle and protein stability in HepG2 hepatoma cells exposed to ferric ammonium citrate (FAC).

127 ificantly up-regulated in obese patients and hepatoma cells exposed to FFA.

128 Hepatoma cells from GNMT mice had defects in LKB1 signal

129 pression of SHP and its co-repressor EID1 in hepatoma cells Huh7, Hepa1, and stellate cells LX2.

130 passage of hepatitis C virus (HCV) in human hepatoma cells in an experimental design in which host c

131 (HCV) in the course of 200 passages in human hepatoma cells in an experimental design that precluded

132 These T cells killed GPC3-expressing hepatoma cells in culture and slowed growth of HCC xenog

133 ases the expression of ATF5 protein in HepG2 hepatoma cells in part by stabilizing the ATF5 protein.

134 HBV-specific T cells lysed HBV-producing hepatoma cells in vitro.

135 nduced metastatic colonization of epithelial hepatoma cells in vivo.

136 nhanced 2-fold in HAP1 and 1.6-fold in human hepatoma cells in which plasminogen receptor (KT) was ov

137 ced 0.35-fold in HAP1 and 0.33-fold in human hepatoma cells in which the plasminogen receptor (KT) wa

138 s9-mediated knockout of CGI-58 in Huh7 human hepatoma cells induced LD deposition and perilipin expre

139 this study, we found that HEV replication in hepatoma cells inhibited poly(I.C)-induced beta interfer

140 The TSLP secreted by HCV-infected hepatoma cells is capable of activating human monocyte-d

141 ent evidence that miR-29 expression in human hepatoma cells is controlled in part by FOXA2, which is

142 that the biotransformation of NPD1 by human hepatoma cells is extremely rapid and faster than that o

143 , coculture of tonsillar cells with infected hepatoma cells lead to an expansion of germinal center T

144 green fluorescent protein (GFP) (E2-GFP) in hepatoma cells led to impaired phosphorylation of IRF-3

145 subcutaneously with AHR-competent Hepa1-GFP hepatoma cells or AHR-deficient LLC lung cancer cells.

146 ll subpopulation, but not in less metastatic hepatoma cells or normal hepatocytes.

147 tenuated IFN-alpha induction by HCV-infected hepatoma cells or TLR ligands, and this inhibitory effec

148 ols, we show the level at which HCV-infected hepatoma cells present endogenously processed HCV epitop

149 As hepatoma cells producing cell culture-derived HCV (HCVcc

150 IFN-alpha induction by HCV-containing hepatoma cells required viral replication, direct cell-c

151 Transient expression of hCH25H in human hepatoma cells restricted HCV infection in a genotype-in

152 We found that RB depletion in hepatoma cells resulted in a compromised immunological r

153 Passage of hepatitis C virus (HCV) in human hepatoma cells resulted in populations that displayed pa

154 BMCs from healthy subjects with HCV-infected hepatoma cells resulted in preferential expansion of cir

155 Silencing of ZNF529 in human hepatoma cells results in upregulation of LDL receptor a

156 Spheroids derived from DCLK1-overexpressing hepatoma cells showed high level expression of active be

157 , forced expression and knockdown of SPZ1 in hepatoma cells showed that SPZ1 was able to regulate the

158 ility in promoting migration and invasion of hepatoma cells than full-length MTA1.

159 with replicons, infectious virus, and human hepatoma cells that express a HCV polyprotein.

160 We cultured hepatoma cells that express luciferase-tagged subgenomic

161 al PC-to-PE ratio and cellular ATP levels in hepatoma cells that expressed various amounts of PEMT.

162 ll proliferation and tumorigenic activity in hepatoma cells through CCND1 induction.

163 tes that constitutive exposure to IFN causes hepatoma cells to become tolerant of ISG function.

164 HCV isolated from culture media of infected hepatoma cells to define viral and host-encoded proteins

165 s (HCV) positive-strand RNA from human Huh-7 hepatoma cells to human plasmacytoid dendritic cells (pD

166 HCV; TNF-alpha increased the permissivity of hepatoma cells to infection by Lassa, measles and vesicu

167 eripheral blood mononuclear cells with Huh-7 hepatoma cells transfected with HCV RNA.

168 expression on LDLR transcript levels between hepatoma cells transfected with the rs6924995 A versus G

169 irus in permissive, transfected human Huh7.5 hepatoma cells upon serial passage.

170 gene was subsequently knocked down in human hepatoma cells using lentiviral vectors expressing small

171 s in mitochondrial metabolism by HepG2 human hepatoma cells using siRNA.

172 cked cell-cycle progression at G2-M phase in hepatoma cells via downregulation of CDK1, induction of

173 IFN-alpha production by HCV-infected hepatoma cells was decreased in pDCs from HCV-infected p

174 ncing of flow-sorted infected and uninfected hepatoma cells we show that the human mucosal immunity g

175 In addition, human hepatoma cells were incubated with different propionate

176 When Huh7 K2040 and Huh7 L2198S hepatoma cells were incubated with IFN-alpha-2a, express

177 Huh7.5.1 hepatoma cells were transfected with small interfering R

178 rat hepatocytes or immortalized H4IIEC3 rat hepatoma cells were treated with lipotoxic levels of pal

179 Human hepatoma cells were treated with Lp(a) purified from hum

180 METHODS AND Human hepatoma cells were treated with Lp(a) purified from hum

181 missing factors, we transduced Huh-7.5 human hepatoma cells with a pooled lentivirus-based human comp

182 Treatment of hepatoma cells with BMP2 induced DGAT2 expression and ac

183 We demonstrate that infection of hepatoma cells with HCV leads to up regulation of the ex

184 Human primary hepatocytes, Huh7 hepatoma cells with silenced PTP1B, mouse hepatocytes fr

185 apacity to replicate efficiently in cultured hepatoma cells without cell culture-adaptive mutations.

186 ) consensus sequences, were viable in Huh7.5 hepatoma cells without requirement for adaptive mutation

187 ion 3-96 h following Tcf7l2 silencing in rat hepatoma cells, and combined this with ChIP-Seq to inves

188 ing of ApoE-deficient TRLs to HSPGs on human hepatoma cells, and decreased clearance of ApoE-deficien

189 ll lines: A549 lung adenocarcinoma and HuH-7 hepatoma cells, and for productive DENV infection of Aed

190 lower than those in highly permissive human hepatoma cells, and minimal infectious particle release

191 -2-induced HBV restriction was weak in Huh-7 hepatoma cells, and the interferon-induced anti-HBV effe

192 Resurrected CSHBV replicated in human hepatoma cells, but human- and tupaia-derived primary he

193 ntly to regulate S6 in an additive manner in hepatoma cells, but it uses mTORC1 as the primary pathwa

194 only 7 (LMO7) is a TGF-beta1 target gene in hepatoma cells, but its role in vascular physiology and

195 higher caspase activation and cell death in hepatoma cells, but not in primary hepatocytes.

196 6C proteins reduced HCV replication in human hepatoma cells, dampening miR-122 stimulation of viral R

197 F19 activated mTORC1 in HepG2 and HuH7 human hepatoma cells, differentiated 3T3-L1 adipocytes and mou

198 apoAIV overexpression increased MTP mRNA in hepatoma cells, indicating transcriptional regulation.

199 zole (BPTT) was most effective against human hepatoma cells, inhibits cell invasion, and decreases ne

200 an be effectively taken up by cultured human hepatoma cells, is nontoxic to the cultured cells and a

201 ion of heparan sulfate biosynthesis in human hepatoma cells, or pharmacological manipulation of hepar

202 tor aminopeptidase N and replicated in human hepatoma cells, suggesting a principal ability to cause

203 In human hepatoma cells, the apo(a) component from the internaliz

204 In human HepG2 hepatoma cells, the rare chr11:47227430 A allele disrupt

205 In contrast, in Huh7 hepatoma cells, the virus must acquire loss-of-function

206 V disables a key receptor ligand in infected hepatoma cells, thereby inhibiting the ability of infect

207 Before infection of naive hepatoma cells, we exposed cell culture-derived HCV stra

208 of cis-proline-containing proteins in human hepatoma cells, we found that combined knockdown of cycl

209 Using primary rat hepatocytes and human hepatoma cells, we found that treatment with the beta-AR

210 nts oleic acid-induced lipid accumulation in hepatoma cells.

211 RNA expression and activity in cultured Huh7 hepatoma cells.

212 on normal mouse NCTC hepatocytes, but not on hepatoma cells.

213 e inflammasome complex in HCV-infected human hepatoma cells.

214 transfecting HBV replication constructs into hepatoma cells.

215 ent was adapted for growth in HepG2C3A human hepatoma cells.

216 1b strain Con1 subgenomic replicon in human hepatoma cells.

217 ed in DNA damage response in hepatocytes and hepatoma cells.

218 ouse brain and approximately 40,000 in human hepatoma cells.

219 eptor tyrosine kinase Axl in EMT-transformed hepatoma cells.

220 host interactions of all ten HCV proteins in hepatoma cells.

221 nced, HBV gene expression and replication in hepatoma cells.

222 duced secretion from primary hepatocytes and hepatoma cells.

223 P-1 and replication assessed after fusion to hepatoma cells.

224 d microdomains purified from hepatocytes and hepatoma cells.

225 domains (NLMs) purified from hepatocytes and hepatoma cells.

226 ows them to recognize and kill GPC3-positive hepatoma cells.

227 of a functional genomics screening in human hepatoma cells.

228 hepatitis C virus (HCV) entry into polarized hepatoma cells.

229 ogenicity and dedifferentiated phenotypes in hepatoma cells.

230 ransferrin (Tf)-receptor-mediated pathway in hepatoma cells.

231 hepatitis C virus (HCV) infection in Huh7.5 hepatoma cells.

232 be linked to cellular cholesterol states in hepatoma cells.

233 ar to that observed with T(3) stimulation in hepatoma cells.

234 tor-beta 1 (TGF-beta1) in HCV-infected human hepatoma cells.

235 IFN-alpha induction in pDCs by HCV-infected hepatoma cells.

236 vimentin, and matrix metalloproteinase-2 in hepatoma cells.

237 olar antiviral activity against HBV in human hepatoma cells.

238 and cell-surface levels of ZIP8 in H4IIE rat hepatoma cells.

239 a but failed to form stable nucleocapsids in hepatoma cells.

240 ess if these miRNAs are actively secreted by hepatoma cells.

241 lar vesicles and HBsAg particles secreted by hepatoma cells.

242 atic energy homeostasis and proliferation of hepatoma cells.

243 ar vesicles and HBsAg particles derived from hepatoma cells.

244 erin, restrict HBV spread in NTCP-expressing hepatoma cells.

245 lk3, ActRIIA, and Hfe, when overexpressed in hepatoma cells.

246 with Pin1-null fibroblasts or PIN1-depleted hepatoma cells.

247 directing T cells to target virally infected hepatoma cells.IMPORTANCE Due to the protective ability

248 examined in a tissue culture model of HCV in hepatoma cells: HCV infection induced extracellular rele

249 otoxicity of nanomaterials to H4IIE-luc (rat hepatoma) cells and HuTu-80 (human intestinal) cells wer

250 o induces Smad1/5/8 phosphorylation in human hepatoma-derived cells and, synergistically with IL-6 an

251 e sought to assess the relationship of serum hepatoma-derived growth factor (HDGF) with PAH disease s

252 during myelination and further investigated hepatoma-derived growth factor-related protein 3 (HRP3 o

253 athway as a functional target of miR-130a in hepatoma-derived Hep3B cells.

254 We recently showed that hepatoma-derived HepG2 cells support the entire HCV life

255 y short-term direct exposure to HCV-infected hepatoma-derived Huh-7.5 cells.

256 Therefore, the hypoxia/hepatoma dual specific gene expression vector with the E

257 this study, we developed a novel hypoxia and hepatoma dual specific gene expression vector.

258 Hepatoma exhibits a series of heterogeneous subpopulatio

259 Treating of rat hepatoma FAO cells with Wy14,643, an agonist of peroxiso

260 dielectric characterization of cancer cells (Hepatoma G2, HepG2).

261 ed the phosphorylation state of JNK1 in both hepatoma H4IIE cells and mouse primary hepatocytes in bo

262 8, and the other expresses low levels (human hepatoma: Hep3B and HepG2; human prostate cancer: PC3 an

263 investigated using the differentiated human hepatoma HepaRG cells.

264 In hepatoma/hepatocarcinoma cell lines, FGFR3 isoforms were

265 In hepatoma/hepatocarcinoma cells, up-regulated FGFR3-IIIb

266 ctivated receptor alpha (PPARalpha) in human hepatoma HepG2 cells and mouse liver.

267 his is based on stable transfection of human hepatoma HepG2 cells with a plasmid that encodes the red

268 uptake and accessible to chromatin in human hepatoma HepG2 cells.

269 nitrogen-containing membrane lipids in human hepatoma HepG2 cells.

270 We analyzed human hepatoma (HepG2) cells and mouse primary hepatocytes to

271 ompatibility was assessed by culturing human hepatoma (HepG2) cells on treated surfaces.

272 e/xanthine and adenine/hypoxanthine in human hepatoma (HepG2) cells were detected simultaneously.

273 ells, but not in mouse liver, cultured human hepatoma (HepG2) cells, or AC16 cultured human cardiomyo

274 Knockdown of Prox1 by siRNAs in human hepatoma Huh-7 cells increased the expression of RORgamm

275 not replicate efficiently in wild-type human hepatoma Huh-7 cells, but it replicates robustly in cert

276 Human hepatoma (Huh-7 and Huh-7.5) and primary HFLCs were incu

277 expected, overexpression of ATGL in cultured hepatoma (HuH-7) cells depleted the cells of LDs, but un

278 ipid droplet content were performed in human hepatoma Huh7 and HepG2 cells using confocal microscopy

279 and FXR isoform expression was confirmed in hepatoma Huh7 and HepG2 cells.

280 ble of transmitting infection to naive human hepatoma Huh7.5.1 cells and establishing a productive in

281 ed exosomes isolated from HCV-infected human hepatoma Huh7.5.1 cells were shown to contain full-lengt

282 t expression of murine GFP-Mx1 in human Huh7 hepatoma, human Mich-2H6 melanoma, and murine NIH 3T3 ce

283 emically or due to mutations repressed it in hepatomas in a dose-dependent manner, whereas beta-caten

284 ose of cisplatin inhibited growth of ectopic hepatomas in mice.

285 ty of LDL-DHA to reduce growth of orthotopic hepatomas in rats.

286 replication and infectivity in Leghorn male hepatoma (LMH) chicken liver cells and in chickens.

287 ression in humans as well as mouse and human hepatoma models of the disease.

288 s highlight ISX as an important regulator in hepatoma progression with significant potential as a pro

289 Incubating McArdle rat hepatoma RH7777 cells with 2-monoacylglycerol caused DGA

290 enhancer and AFP promoter may be useful for hepatoma specific gene therapy.

291 usly demonstrated that the CD133(-)/EpCAM(-) hepatoma subpopulation was more metastatic than its coun

292 ly expressed gene clusters upon encountering hepatoma target cells presenting endogenously expressed

293 f hepatocellular carcinoma (HCC, also called hepatoma) therapy.

294 fectoprotein (AFP) promoter and enhancer for hepatoma tissue specific gene expression.

295 A high positive correlation existed in human hepatoma tumors between ISX and CCND1 expression.

296 Human hepatoma up-regulated protein (HURP) is a substrate of A

297 lic steatosis and in ethanol-incubated human hepatoma VL17A cells.

298 ents (death, decompensation, transplant, and hepatoma) were evaluated, and Kaplan-Meier survival esti

299 n = 15) and tumor growth in a remote BNL 1ME hepatoma xenograft tumor (n = 28).

300 transduction efficiency of dcAd5-CMV/NIS in hepatoma xenografts.